Hydrocephalus associated with long term spaceflight (HALS) for missions lasting over five months is well described but poorly understood. While structural changes of the brain due to microgravitational forces affecting the circulation of cerebrospinal fluid (CSF) have been described as one potential cause, we propose an alternative hypothesis based on dynamic disequilibrium of macromolecular transport across the blood brain barrier. We propose that factors altering physiology under conditions of spaceflight such as microgravity, hypercapnia, venous hypertension, medications, and dietary substances contribute to increased protein load in the ventricles and/or contribute to impairment of transport out of the ventricles that results in HALS. Individual variation in the genetic expression of efflux transporters (p-glycoprotein) has been shown to correlate with the presence and degree of hydrocephalus in animal studies. We describe the evidence behind this concept and propose how these factors can be studied in order to determine the underlying pathogenesis which is imperative in order to cure or prevent HALS.

与持续五个多月的任务的长期太空飞行 (HALS) 相关的脑积水被很好地描述但知之甚少。虽然由于微重力影响脑脊液 (CSF) 循环而引起的大脑结构变化已被描述为一个潜在原因，但我们提出了一种基于大分子跨血脑屏障动态不平衡的替代假设。我们提出，在太空飞行条件下改变生理机能的因素，如微重力、高碳酸血症、静脉高压、药物和膳食物质，会导致心室蛋白质负荷增加和/或导致心室外运输受损，从而导致 HALS。在动物研究中，外排转运蛋白（p-糖蛋白）基因表达的个体差异已被证明与脑积水的存在和程度相关。我们描述了这一概念背后的证据，并提出了如何研究这些因素以确定潜在的发病机制，这对于治愈或预防 HALS 是必不可少的。